The sensory neuropeptide calcitonin gene-related peptide (CGRP) is a potent microvascular vasodilator (Brain et al. 1985). CGRP receptors are comprised of the seven transmembrane GPCR, the calcitonin-like receptor (CLR), a receptor activity-modifying protein 1 (RAMP1) molecule and an intracellular protein, known as the receptor component protein (RCP). Previous work in our laboratory has shown that genetic deletion of aCGRP in mice leads to increased susceptibility to elevated blood pressure and associated vascular remodeling in an Ang II model of hypertension. We now investigate the role of CGRP within the cardiovascular system of the ageing mouse. Male and female aCGRP wild type (WT) and knockout (KO) mice were used, aged 15 months, and juveniles aged 3 months. Blood pressure measurements were taken via tail cuff (Kent Scientific) for one week following a one-week training protocol. Heart rate was determined by pulse oximetry (Kent Scientific). Mice were killed via induction of anaesthesia and subsequent cervical dislocation. We characterised potential gross organ pathology by measuring body weights and organ weights, including heart and kidney. Aortae were processed into paraffin blocks for histology (Masson’s trichrome). Aortic mRNA expression of CGRP receptor constituents were analysed by RTqPCR. Raw data were normalized to reference genes and data were expressed as copies per microliter of sample. All data are expressed as mean ± SEM and data were interrogated by two-tailed unpaired t-test or one-way ANOVA, where appropriate. A level of p < 0.05 was deemed to be statistically significant. Both WT and KO animals aged 15 months did not appear to display any gross organ pathology and did not differ with respect to cardiac or renal hypertrophy as determined by weight. Furthermore, we found no differences in baseline blood pressure in aged aCGRP WT and KO mice (mean arterial pressure 105.1 ± 4.1 and 104.9 ± 3.0 mm Hg, respectively, n=6). We also have shown a trend towards an increased mRNA expression of RAMP1 in KO mice (25.71 ± 21.59 vs 270.4 ± 183.9 copies/ul) and a significant increase in CLR mRNA in KO aortic tissue (1,775 ± 1,163 vs 6,732 ± 1,977 copies/ul, two tailed unpaired t-test, P < 0.05, n=4) was also observed. RCP expression appeared to be unchanged between groups (3,564 ± 1,404 vs 16,024 ± 10,188 copies/ul). In conclusion, we provide new evidence showing that genetic deletion of aCGRP appears to have little effect on gross organ pathology as animals age to 15 months. Furthermore, we have shown that CGRP appears to have little role to play in the regulation of blood pressure both at baseline in juvenile animals and as age progresses. This minimal effect of CGRP deletion on haemodynamics occurs in spite of an apparent increase in CGRP receptor constituent gene expression.